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NUR 521 Exam 1 Blueprint and Study Guide Module 1:Foundational Principles of Pharmacotherapeutics There are no prototype drugs in module 1. 1. Legal issues a. Why should APRNs have full prescriptive authority? Who would benefit from this?...
NUR 521 Exam 1 Blueprint and Study Guide Module 1:Foundational Principles of Pharmacotherapeutics There are no prototype drugs in module 1. 1. Legal issues a. Why should APRNs have full prescriptive authority? Who would benefit from this? i. APRNS should have full authority so that they can meet the demands for future healthcare needs. Without it, groups in areas of the greatest need may not get the care they need. 2. Controlled Substance Classification a. What is the definition of each schedule of drugs? Can you provide an example drug that fits in each schedule? i. Schedule I: No acceptable medical use with high abuse potential ex: Heroin, marijuana, LSD, MDMA ii. Schedule II: narcotic stimulants and depressants w/ high abuse potential and severe psychic or physical dependence liability ex: opium, morphine, dilaudid, methadone, Demerol, hydrocodone iii. Schedule III: Abuse potential, less than I or II, and contain compounds w/ limited quantities of certain narcotics ex. products w/ no more than 90 mg of codeine such as Tylenol w/ codeine, buprenorphine (Suboxone) iv. Schedule IV: Abuse potential less than those in III ex. barbital, phenobarbital, Xanax, Domalin, chloral hydtrate, clorazepate v. Schedule V: less abuse potential than IV and contain preparations containing limited quantities of certain narcotic and stimulants used for cough, diarrhea, and pain ex. buprenorphine and propylhexedrine. 3. Prescribing Medications a. What components are necessary when writing a prescription? i. Prescriber name, license number, and contact information ii. DEA number when needed. iii. NPI number iv. Patient name and DOB v. Patient allergies vi. Name of medication vii. Indication of use for medication viii. Medication concentration ix. Dose, route, frequency x. Number of tablets to dispense. xi. Number of refills xii. If okay to use generic form of medications b. What factors should the APRN consider when prescribing medications? i. Cost and availability ii. Guidelines iii. Interactions and side effects iv. Allergies v. Liver and renal function vi. Monitoring parameters vii. Special populations viii. Never pre-sign scripts ix. Do not use abbreviations. x. Write in ink and use temper-resistant scripts. c. What factors should the APRN consider when refilling medications? i. Is this a new medication for the patient? ii. Am I changing the dose or frequency? iii. Am I adding new medications to their regimen? iv. Is the patient having undesired side effects? v. When do I expect to follow up with this patient? vi. When was the last time I saw this patient? Do I need to see them again before refill? vii. Is this a schedule II medication? These are not eligible for refills and need a new prescription each time. d. What is the benefit of collaboration during drug selection and prescription writing? i. Helps to develop a relationship with the pharmacist, who can provide additional information. They have firsthand knowledge of formulary and can assist with dosing. ii. Also helps to have an ID specialist because they know more options available to the patient. 4. Patient Education a. What information should be included in patient education materials? i. Name of medication ii. Purpose iii. Dose iv. Administration v. Adverse effects vi. Storage vii. Laboratory testing viii. Interactions ix. Duration of therapy b. Why is patient education so important? i. Medication information can be easy to forget, especially for a patient taking multiple medications. Education is the best way to promote positive outcomes with drug therapy. Make sure to teach patients common side effects as well as severe issues such as pancytopenia or liver injury. Teach patient signs and symptoms of these side effects and when they need to report them. 5. Promotion of Safe Outcomes (drug monitoring and adherence) a. What is the best way to promote positive outcomes with drug therapy? i. Selecting and prescribing the most appropriate drug for the patient and providing them with appropriate education regarding that medication. b. Why do we monitor drug therapy? i. Determining therapeutic dosage ii. Evaluating medication adherence iii. Identifying adverse effects c. What are some reasons that a patient will not take their medications? How can you address these as a provider? i. Forgetfulness ii. Lack of planning iii. Cost iv. Dissatisfaction v. Altered dosing 6. Pharmacokinetics, Pharmacodynamics, and Drug Interactions a. Pharmacokinetics: science that analyzes how the human body interacts with a drug; “What the body does to the drug” b. Pharmacodynamics: science that studies the biochemical and physiologic effect of a drug and its organ-specific mechanism of action, including effects on a cellular level; “What the drug does to the body” c. Be able to define each of the four processes: absorption, distribution, metabolism, and excretion. i. Absorption: movement of a drug from its site of administration into the blood or systemic circulation; rate of absorption determines how fast the effects are and the amount of absorption determines the intensity of the effects. ii. Distribution: drug’s movement from the blood to the interstitial space of tissues and from there into cells and to the site of drug action iii. Metabolism: enzymatic mediated alteration of a drug structure. Most are metabolized in the liver via the P450 system. iv. Excretion: movement of drugs and their metabolites out of the body. Elimination is a combo of excretion and metabolism. d. What is bioavailability? i. Bioavailability: the amount of an active drug that reaches the systemic circulation from its site of administration. e. What are some factors that can affect bioavailability? i. Genetics ii. Gender iii. Race f. Explain how the same drug manufactured by different drug companies can have different absorption rates. i. Two formulations of the same drug can be chemically equivalent while differing in bioavailability. The inactive ingredients used by drug companies are called binders and fillers. These ingredients can dissolve at different rates affecting the bioavailability of the drug. The patient themselves can also have different metabolisms, gastric emptying times, etc. g. What happens when a patient takes a drug that is metabolized by p450 enzymes if an inducing OR an inhibiting drug is added to the current drug regimen? h. Most drugs are metabolized via the hepatic microsomal enzyme systems (P450). This refers to cytochrome P450, a key component in this enzyme system. Drugs that are metabolized by this system are called substrates. If taken with an inducer, the rate of metabolism of the drug will be increased. If taken with an inhibitor, the rate of metabolism of the drug will be decreased. i. What is the difference between an agonist and antagonist? i. Agonists: molecules that activate receptors. Drugs that are agonists bind to receptors and mimic the action of the body. Agonists have high affinity and high intrinsic activity. Ex. Dobutamine ii. Antagonist: prevent receptor activation by endogenous regulatory molecules and drugs. These drugs can attach to receptor sites but prevent activation of the receptor. They prevent the body’s response. Ex. antihistamines iii. Partial agonists: can be both. These work through physical or chemical interactions. Ex. antacids, antiseptics, saline laxatives. j. What drug interaction clinical pearl did you learn from this lecture? i. The safest practice is to check for drug interactions in a reliable software application. 7. Adverse Drug Reactions a. What are ways to minimize adverse drug reactions? i. Monitor kidney, liver, and bone marrow function through labs. ii. Monitor signs and symptoms. iii. FDA special alerts: medication education, black box warnings, risk evaluations and mitigation strategy (REMS) to minimize drug-induced harm. b. How do you handle a patient complaint about a side effect of a medication? i. If it is a new symptom, suspect the drug is the cause. Report the effect to MedWatch, the FDA Medical Products reporting Program. Be sure to investigate before reporting. Be sure to address the patient’s concerns. 8. Medication Errors a. What are factors that contribute to medication errors? How can a provider minimize the risk for medication errors? i. Prescribing practices: wrong drug, error in dose, lack of clear instructions, illegible writing ii. Oversight: failure to have up-to-date med list, failure to continue of DC meds, absence of medication reconciliation iii. Communication: inadequate or unclear, failure to verify sound alike drugs, inadequate patient education 9. Individual Drug Responses a. Think about patient scenarios where each of the individual variations in drug response may occur. i. Body weight: concentration of drug at its sites of action (very important in peds) ii. Age: infants and older adults are more sensitive; older adults also have comorbidities and multiple drugs being prescribed iii. Physiologic alterations: kidney disease, liver disease, acid-base imbalance, altered electrolytes. iv. Bioavailability: different formulations of the same drug; tablet disintegration time, enteric coatings, and sustained-release meds v. Gender and race: genetically based. 1. Gender a. Women not included in FDA studies until 1997. b. Digoxin can increase mortality in women w/ no effect on men. c. Alcohol metabolizes more slowly in women than men. d. Certain opioids (pentazocine, nalbuphine) are more effective on women and can achieve pain relief at a lower dose. e. Quinidine causes greater QT interval prolongation in women; more likely to develop torsades de pointes, a fatal cardiac dysrhythmia. 2. Race a. BiDil, a fixed-dose combo of two vasodilators (ISDN and hydralazine) was approved for AA population only. vi. Comorbidities 1. Two or more medical conditions, meaning drugs taken to manage one may affect another. Example: asthma and HTN> non-selective beta blocker to control BP may worsen a patient’s asthma through airway constriction. 10. Genetic Considerations a. What is the purpose of genetic testing? i. To study the genetic variations of an individual that affect individual responses to drugs through alterations in genes that code for drug metabolizing enzymes and drug receptors. b. Provide examples of genetic variations that affect drug responses. i. CYP2D6: Tamoxifen reduced therapeutic effect; women with inadequate of this gene activity cannot convert Tamoxifen to its active form, preventing protection from breast cancer. Consider hormonal therapy or differing doses of the Tamoxifen. ii. HER2 overexpression: Trastuzumab (Herceptin) increased therapeutic effects); Herceptin only acts against breast cancers that overexpress HER2. 11. Drug Therapy Across the Lifespan (pregnancy, breast feeding, older adults) a. When are pregnant women most susceptible to teratogenic drugs? i. During the embryonic period (roughly the first trimester). This is when the shape of internal organs and other structures are being established. Teratogens exposure in the second and third trimester usually affect function rather than gross anatomy, ex: learning deficits and behavioral abnormalities. b. What are ways to minimize drug concentrations in breast milk? i. Lipid soluble drugs readily enter breast milk while ionized, highly polar, or protein bound tend to be excluded. ii. Dose immediately after breast feeding to minimize drug concentration in milk at next feeding. iii. Avoid drugs that have a long half-life. iv. Avoid sustained release formations. v. Choose drugs that tend to be excluded from breast milk. vi. Choose drugs that are least likely to affect the infant. c. What affects frug metabolism in pediatric patients? i. Renal drug excretion is lower in infants. ii. Pharmacokinetic processes are immature and take longer to process drugs until approximately one year of age. iii. Drugs without pediatric dosing is based on body surface area (BSA); Child’s BSA x adult dosage divided by 1.73 m2+ pediatric dose. iv. Pediatric dosing is based on body weight. d. What changes occur in the organ function of older adults? How would this affect medications? i. Altered pharmacokinetics and variable drug sensitivities to multiple co- morbidities. ii. Multidrug therapies iii. Poor adherence iv. Absorption of drugs 1. Increased gastric pH, decreased absorption surface area, decreased blood flow, decreased GI motility, delayed gastric emptying. v. Distribution of Drugs 1. Increased body fat, decreased lean body mass, decreased total body water, decreased serum albumin, decreased cardiac output. vi. Metabolism of Drugs 1. Decreased hepatic blood flow, decreased hepatic mass, decreased activity of hepatic enzymes. vii. Excretion of Drugs 1. Decreased renal blood flow, decreased glomerular filtration rate (GFR), decreased tubular secretion, decreased number of nephrons. e. How do you calculate GFR? i. The proper index of renal function in older adults is creatinine clearance- serum creatinine levels alone do not accurately reflect kidney function in older adults due to a decrease in lean muscle mass. ii. GFR shows how well the kidneys are filtering. Creatinine is a waste product that comes from digestion of dietary protein and the normal breakdown of muscle tissue. iii. Normal GFR results: > 90 but can lower some with ages over 70 years. iv. You must have the serum creatinine, patient age, ethnicity, and race. 12. Beers Criteria a. What is this and why would you use it? b. Beers criteria is a list of medications with a high likelihood of severe adverse effects that you want to avoid using patients over the age of 65. c. Provide an example of when applying this information when prescribing medications would be helpful. i. Five Beers Criteria 1. Medications to avoid if you are over 65 and not in a hospice or palliative setting. 2. Medications to avoid among people with certain health conditions. 3. Medications to avoid that cause drug interactions when combined with other medications. 4. Medications to avoid due to harmful side effects that outweigh the benefits. 5. Medications to use at limited doses or avoided due to effects on kidney function. Module 2: Neuropharmacy and Pain 1. Drugs to Known a. Know the MOA, Use, common adverse effects, serious adverse effects, dosing, administration, CI, interactions, and patient education. 2. Foundations of Neuropharmacology a. The study of drugs that alter processes controlled by the nervous system. b. These drugs produce the same effect of natural neuronal activity on the body. c. Nervous system regulates all bodily processes. 3. Peripheral Nervous System a. Two major subdivisions: somatic motor system and the autonomic nervous system b. Autonomic nervous system: regulation of the heart, regulation of secretory glands, regulation of smooth muscles c. Autonomic nervous system is further divided into the parasympathetic nervous system and the sympathetic nervous system. d. Parasympathetic Nervous System i. “Rest and Digest” ii. Slowing heart rate, increased gastric secretions, emptying of bladder/bowel, focusing the eye for near vision, constricting the pupil, constricting bronchial smooth muscle. e. Sympathetic Nervous System i. “Fight or flight” ii. Regulating CV system, regulating body temperature, acute stress response iii. CV: increasing cardiac output and vasoconstriction of arterioles and veins iv. Maintains and redistributes blood flow to brain and body v. Promote sweating and dilating surface vessels vi. Increase heart rate and BP, dilating bronchi, dilating pupils, mobilizing stored energy (glucose and fatty acids to muscles) 4. Neurotransmitters a. Acetylcholine: employed at most junctions in the PNS, sweat glands, skeletal muscles b. Norepinephrine: released by almost all postganglionic neurons of SNS. c. Epinephrine: released by adrenal medulla d. Dopamine 5. Receptors of Peripheral Nervous System a. Cholinergic receptors: mediate responses to Ach. i. Nicotinic N, nicotinic M, and muscarinic ii. Nicotinic M: contraction of skeletal muscles iii. Muscarinic: increased gland secretions, contraction of smooth muscle in bronchi and GI tract, slow HR, pupil constriction, focus for near vision, dilation of blood vessels, voiding of bladder (contract detrusor and relax sphincter). b. Adrenergic receptors: mediate responses to epinephrine and norepinephrine. i. Alpha 1 and 2, beta 1 and 2; and dopamine. ii. Alpha 1: eyes (pupil dilation), vasoconstriction, male ejaculation, contraction of bladder and prostate iii. Alpha 2: don’t worry about iv. Beta 1: increase HR, force of contraction and velocity of AV node; renin elevates BP v. Beta 2: bronchial dilation, relaxation of uterine smooth muscles, vasodilation, breakdown of glucose (higher blood sugar levels), muscle contraction vi. Dopamine: increase renal perfusion through blood vessel dilation c. Acetylcholine can activate all 3 receptors. d. Epinephrine can activate all alpha and beta receptors, but not dopamine. Epinephrine is the only one to act on beta 2 receptors. i. Causes fight or flight response, dilation of blood vessels in heart, lungs, and skeletal muscles and increasing blood flow to these organs. Dilate bronchi, increasing oxygen, increase glucose available, relax uterine smooth muscles, preventing delivery. e. Norepinephrine can activate alpha 1 and 2 and beta 1, but not beta 2 receptors. f. Dopamine can activate alpha 1, beta 1, and dopamine receptors. 6. Cholinergic Drugs (Activate PNS) a. Muscarinic Agonist: mimics effects of acetylcholine binding; PNS response i. Bradycardia, sweating, salivation, increased secretions ii. Contraction of muscles in lungs and GI tract iii. Release of urine, pupillary constriction, and near vision iv. Across the lifespan: Not safe in peds, pregnancy, or breastfeeding 1. Watch in older adults due to decreased hepatic, cardiac, and renal function v. Bethanechol (Urecholine): used for urinary retention in postop and postpartum and neurogenic atony of bladder vi. Muscarinic toxicity: diaphoresis, urination, miosis, brady, bronchospasm, emesis, lacrimation, salivation: give atropine to reverse b. Cholinesterase Inhibitors c. Prevents breakdown of acetylcholine, therefore enhancing cholinergic action. i. Used to treat MG, glaucoma, Alzheimer’s, Parkinsons, poisoning by muscarinic antagonist, and reversal of neuromuscular blockade ii. Across the lifespan: not safe in kids, maybe necessary when treating MG in pregnancy and labor, older adults get it for its associated with dementia and Alzheimer’s iii. Pyridostigmine (Mestinon) 1. Treatment of MG: you know it is working when your patient is able to have increased strength and muscle control 7. Muscarinic Antagonists (SNS-type reaction) a. Blocks the action of acetylcholine (blocking the PNS) b. Do not use in older adult due to potential to cause confusion, blurred vision, tachycardia, urinary retention, and constipation. Combined with co-morbidities, leaves geriatric patients at higher risks for complications. c. Atropine (Atropen): prevents bradycardia in surgery, antidote to muscarinic poisoning, sinus bradycardia and AV block, long term ophthalmic preparations. i. Increases HR, decreases secretions and salivation, relaxes bronchi, decreases tone of GI tract and bladder, pupil dilation and lens focus ii. Can precipitate acute glaucoma, myasthenic crisis, or urinary retention iii. Antidote: physostigmine iv. Toxicity: hot as a hare, dry as a bone, red as a beet, blond as a bat, mad as a hatter 8. Adrenergic Agonist (SNS-type reaction) a. SNS drugs i. Alpha 1: vasoconstriction and mydriasis ii. Alpha 2: do not worry about iii. Beta 1: increase HR and force of contraction iv. Beta 2: bronchodilation and uterine relaxation and glucose breakdown b. Across the lifespan: used in peds in emergency situations, pregnancy can decrease oxygen to the fetus, breastfeeding use caution, and older adults have an increased risk for adverse effects c. Epinephrine: delay local anesthetics, control superficial bleed, elevate BP, AV heart block, cardiac arrest, asthma, anaphylactic shock d. Using an Epi-pen: 0.3 or 0.5 mg and may repeat every 5 to 15 mins if patient does not respond to first dose. Call 911 during administration. Not more than 2 sequential doses without supervised medical attention. 9. Adrenergic Antagonists a. Causes direct blockage of adrenergic receptors b. Across the lifespan: only certain ones approved for pediatric use, drugs approved are for BPH, so not usually seen in pregnancy and breast feeding, Beers criteria due to orthostatic hypertension c. Prazosin (Minipress): dilates arterioles and veins and relaxes smoother muscle of bladder and prostate; treatment for HTN (not DOC), BPH, Raynaud’s, PTSD d. Be aware of first dose affect and orthostatic and postural hypertension. 10. Centrally Acting Alpha 2 Agonists a. Selective activation of alpha 2 receptors in the CNS: produces vasodilation and bradycardia b. Mainly used to treat hypertension. Can also be used for severe pain and ADHD. c. Across the lifespan: kids above 6 years old, avoid in pregnancy and breastfeeding, and Beers criteria for patients over 65 d. Causes CNS depression: drowsiness, rebound hypertension, dry mouth, high abuse potential e. Education: take most doses at night to minimize sedation during the day 11. Central Nervous System a. 21 different neurotransmitters i. Monoamines, amino acids, purines, opioid peptides, nonopioid peptides, acetylcholine, and histamine b. Different drugs effects based on the brain’s ability to adapt. 12. Parkinson Disease a. Ideal treatment does not exist; only symptomatic relief. They do not cure PD. b. Too little dopamine and too much acetylcholine. c. Medical treatment works to activate dopamine receptors and block receptors for acetylcholine. d. Levodopa/Carbidopa: cornerstone for PD treatment. Levodopa increases dopamine synthesis and carbidopa inhibits breakdown of levodopa e. Full therapeutic response can take a few months to reach and after t years, the medication stops working as well. f. Know it is working: improvement in ability to perform ADLs independently. g. Avoid high protein meals, get up slowly, and the drug can induce psychosis, where clozapine may be needed for treatment. h. Drug that prolongs the half-life of Levodopa: Entacapone i. You can also shorten the dosing interval or give a direct-acting dopamine agonist such as Ropinirole (Requip) i. Ropinirole (Requip): direct dopamine agonist i. Used to treat restless leg syndrome by activating D2 and D3 receptors which helps to control muscle movement. ii. When combined with Levodopa/Carbidopa, can result in dyskinesias, hallucinations, and postural hypotension. 13. Alzheimer’s Disease a. Two main drugs discussed used to treat Alzheimer’s: Donepezil (Aricept) and Memantine (Namenda) b. Donepezil (Aricept) i. Reversible inhibition of acetylcholine makes more acetylcholine available, improving communication cells in the brain, improving memory and cognition. ii. Contraindicated in high degree heart blocks iii. Long half life, but takes up to 15 days to achieve steady state; well absorbed and metabolized by the liver. Stay on dose 11-3 months before increasing iv. Causes cholinergic affects: increased secretions, increased muscle contractions, decreased HR, weight loss c. Memantine (Namenda) i. Moderates glutamate (excitatory NT) at NMDA receptors (critical role in learning and memory) ii. Severe hepatic impairment issues and can cause corneal issues to worsen iii. Slow the decline of AD and possible symptom improvement iv. Adjust dosing for renal impairment 14. Seizure Disorders a. Phenytoin (Dilantin) i. Selective inhibition of sodium channels results in decreased action potentials ii. Used for partial and generalized tonic-clonic seizures NOT absence. iii. Test for HLA B *1502 gene mutation: TENS or SJS reaction iv. No stopping abruptly v. Narrow therapeutic index: 10-20 vi. CNS effects, gingival hyperplasia, rash, hirsutism vii. Neural tube defects in pregnancy b. Oxcarbazepine (Trileptal) i. Blocks sodium channels in neuronal membranes derivative of Tegretol ii. Monotherapy and adjunctive for partial seizures iii. Can worse osteo-conditions iv. CNS depression v. Do not stop abruptly; neural tube defect in pregnancy. vi. Oral contraceptive issues 15. Muscle Spasms and Spasticity a. Baclofen (Lioresel) i. Suppress hyperactive reflexes involved in regulation of muscle movement ii. Reduce muscle spasticity associated with MS and spinal cord injury (preferred over Dantrolene) iii. BBW: abrupt withdrawal results in high fever, AMS< rebound spasticity, muscle rigidity, rhabdomyolysis, MOSF, and death iv. Start with smaller doses and gradually increase; do not stop suddenly b. Dantrolene (Dantrium) i. acts on skeletal muscles by suppressing calcium release, decreased muscle contraction. ii. Spasticity due to spinal cord injury or CNS condition iii. Contraindicated in liver disease iv. BBW: Fatal hepatotoxicity c. Cyclobenzaprine (Amrix) i. Centrally acting skeletal muscle relaxant; relief of muscle spasm and associated pain ii. Use with MAOIs within 2 weeks: can lead to serotonin syndrome 1. Serotonin syndrome: too much serotonin built up in the body. Signs and symptoms are stiff muscles, confusion, agitation, restlessness, N/V, dry membranes, flushed skin iii. CNS depressant, anticholinergic effects 16. Local Anesthetics a. Lidocaine: localized pain relief; blocks sodium channels b. Do not combine with epinephrine; risk for necrosis in certain body areas c. CNS excitement and then depression d. CV can affect heart and blood vessel; can cause brady, heart block and even cardiac arrest in extreme situations. e. Risk for injury due to numbness 17. Opioid Analgesics a. Morphine i. Pain relief by activating mu receptors in CNS ii. Contraindications: respiratory depression issues (CNS depression) iii. Adverse effects: constipation, orthostatic hypotension, urinary retention, N/V, sedation, neurotoxicity, tolerance iv. Opioid overdose: Narcan b. Naloxone (Narcan) i. Competitive antagonist at opioid receptors ii. Reversal agent for opioid agonist (resp depression, coma, analgesia) iii. IM, IV SQ: 0.4 to 2 mg, repeat every 2-3 minutes iv. ½ life is 2 hours v. If no response after 10 mg, consider other causes of respiratory depression vi. Intranasal: 4 or 8 mg as single dose in one nostril, repeat every 2-3 minutes in alternating nostrils 18. Headache a. Imitrex i. Selective activation of serotonin receptors causing vasoconstriction ii. Aborts ongoing migraine iii. Teratogenic in pregnancy, ischemic heart conditions, MI, or uncontrolled HTN iv. Adverse effects: bad taste in mouth, coronary vasospasm (angina) v. SSRI use can lead to serotonin syndrome Module 3: Psychiatric Mental Health 19. Neurotransmitters in Psych a. Dopamine: influences how we interact with the world. Found in all areas of the brain. Involved in psychosis. (Schizophrenia, bipolar, Alzheimer’s) b. Norepinephrine: excitatory impact (fight or flight); major role in mediating mood and anxiety; regulation of NE is generally used in treating mood and anxiety disorders. (Major depression, bipolar, Alzheimer’s, anxiety) c. Serotonin: influence temperature, sensory, sleep, and assertiveness areas of the brain. Serves as chemical mediator in pain perceptions, normal and abnormal behaviors, moods and drives, regulation of food intake, and neuroendocrine functions. (Major depression, bipolar, Alzheimer’s, anxiety) d. GABA: chemical made in the brain. It is an inhibitory NT that reduces a nerve cells’ ability to send and receive chemical messages through CNS. Linked with anxiety, autism, and Parkinson’s (bipolar, anxiety) e. Acetylcholine: first NT; plays a major role in encoding memory and cognition. (Alzheimer’s, bipolar) 20. Classic adverse reactions associated with first generation antipsychotic medications: a. Orthostatic hypertension, prolonged QTc interval, anticholinergic, weight gain, diabetes, sexual side effects, blood disorders (agranulocytosis), neuroleptic malignant syndrome (NMS), photosensitivity, lowered seizure threshold, medication-related movement disorders 21. Education the NP should provide to the patient and family regarding possible side effects and patient monitoring when prescribing clozapine. a. Blocks receptors for serotonin and dopamine. b. Used for schizophrenia and reducing suicidal behavior when other drugs have failed. Monitor CBC, cardiovascular exam, and blood glucose. c. Adverse effects include sedation, weight gain, lowered BP, anticholinergic effects, new onset diabetes, dyslipidemia, and seizures d. BBW: agranulocytosis and myocarditis e. Rare effects: NMS, photosensitivity, and a lowered seizure threshold. 22. Explain how the NP manage sexual dysfunction caused by antidepressant medications. a. Reducing the dosage of the medication of witching to a high potency FGA may reduce adverse effects. Examples include Haldol, 23. Why should MAOIs and SSRIs not be taken together? How would you prevent complications from changing psychiatric medications when discontinuing one and starting another? a. Combining MAOIs and SSRIs leaves a patient vulnerable to serotonin syndrome. b. The original antipsychotic should be tapered off to nothing, followed by a washout period (will be based on the half life of the medication the person had originally been on), and then begin a slow and tapered start dose of the second medication. 24. What patient education should be covered when starting an MAOI and why? a. The greatest risk for these patients is hypertensive crisis (headache, tachycardia, hypertension, nausea, vomiting, confusion, and profuse sweating) due to eating foods high in tyramine. MAOI does not allow the body to process tyramine correctly, leading to an excess build up of it in the body. Tyramine releases norepinephrine from sympathetic neurons. This in turn causes massive vasoconstriction and intense stimulation of the heart. 25. What conditions does Risperidone treat? a. BPD manic episodes 26. What does Lithium treat? a. Mania and depressive episodes of bipolar illness 27. Are Risperidone and Lithium ever used in combination? a. Lithium is used as a mood stabilizer and is combined with risperidone to help control symptoms during an acute manic episode. Lithium helps stabilize the mood itself with risperidone helps control the symptoms of mania. 28. Signs and symptoms of serotonin syndrome a. Mental status changes (hallucinations, agitation), autonomic instability (tachycardia, hyperthermia, BP changes), neuromuscular problems (hyperreflexia, incoordination), Gi disturbances (N/V/D); can be life-threatening. 29. Signs and symptoms of drug withdrawal a. Dilated pupils, increased vital signs, physical fatigue, rhinorrhea, sleep disturbances, N/V, cramping, diarrhea, anxiety, irritability, and depression. 30. Conditions that may develop as a result of taking lithium and their treatments a. Tremors: use divided doses, sustained release doses, or a beta blocker b. Polyuria: take amiloride, a potassium sparring diuretic, and make sure to stay hydrated. c. Goiter and hypothyroidism: measure levels, adjust dosing, take Synthroid d. Lithium toxicity: hemodialysis if necessary 31. Durg of choice for different types of mania a. Pure manic episode (Euphoria mania): mood stabilizers, seven second generation antipsychotics, and a benzodiazepine if needed. b. Hypomanic Episode (hypomania): no required treatment c. Major depressive episode (Depression): mood stabilizers, atypical antipsychotic, or a mood stabilizer/antipsychotic plus an antidepressant d. Mixed Episode: significant risk for suicide 32. Drug of choice for depression a. SSRI: Fluoxetine (Prozac): anticholinergic effects 33. Drug of choice for panic attacks a. SSRI (Prozac) or SNRI (venlafaxine): nausea, diarrhea, fatigue, and drowsiness b. Benzodiazepines are also a first choice treatment for anxiety disorders. Examples include Xanax, Valium, and Ativan as well as Temazepam and Triazolam. 34. Which psychiatric medications potentiate asthma? a. Typical antipsychotics (clozapine) as well as anticholinergics (amitriptyline) and imipramine can worsen the symptoms of asthma. 35. What health information should be monitored in patients receiving methylphenidate? a. Considered to be an amphetamine. b. Release of norepinephrine and dopamine. c. Increase wakefulness, alertness, mood, stimulate respiration, decrease appetite, increase heart rate, and have high potential for tolerance as well as abuse. d. Can cause insomnia and restlessness, weight loss, and increased HR and BP, which can cause issues in patients with previous cardiac disorders. e. Excessive use can cause paranoid psychosis. 36. What labs should be monitored in a patient taking lithium? a. Blood levels for toxicity (0.8-1.2 mEq/L), creatinine concentrations, thyroid hormones, and BCB every 6 months 37. What is substance abuse disorder? a. A cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance despite significant substance-related issues. Although physical dependence can contribute to addictive behavior, it is neither necessary not sufficient for addiction to occur. 38. What medications should patients with alcohol abuse disorder not take? a. CNS Depressants: CNS depression b. NSAIDs: injury to GI mucosa resulting in significant gastric bleeding c. Acetaminophen: potential for fatal liver injury. d. Disulfiram (Antabuse): effects used to help maintain abstinence e. Antihypertensive drugs: alcohol raises BP, and so it counteracts the effects of antihypertensive medications 39. What are the sequelae of long-term alcohol abuse? What body system does alcohol adversely affect? a. Wernicke’s encephalopathy: lack of thiamine. Causes confusion, nystagmus, and abnormal ocular movements. Readily reversible with thiamin. b. Korsakoff psychosis: polyneuropathy, inability to convert short term to long term memory, and confabulation. Is not reversible. c. Most dramatic long term effect: enlargement of cerebral ventricles, in response to atrophy of cerebellum itself. Impairment of memory and intellectual function. Only partially reversible. 40. What are the physical manifestations of cocaine abuse, ecstasy abuse, marijuana abuse, and methamphetamine abuse? What about S/S of overdose in each of these agents? a. Cocaine abuse: euphoria similar to amphetamines through uptake of dopamine. i. Toxicity: agitation, dizziness, tremor, blurred vision. Hyperpyrexia, convulsions, ventricular dysrhythmias, and hemorrhagic stroke. Anxiety, paranoia, and hallucinations. b. Ecstasy abuse: euphoria, psychedelic effects in low dose and amphetamine-like effects in high doses i. Toxicity: neurotoxicity, seizures, excessive cardiac stimulation, and hyperthermia c. Marijuana abuse: euphoria, sedation, and hallucinations. Increased sensitivity and humor, delusions. i. Toxicity: antimotivation syndrome, cannabinoid hyperemesis syndrome, increased HR, orthostatic hypotension and reddening of conjunctiva, bronchodilation, but constriction of airway with chronic use, decreased sperm count, reduction in size of hippocampus and amygdala. d. Methamphetamine abuse: increases norepinephrine and dopamine uptake. Produces arousal and elevation of mood, euphoria, and talkativeness. Increased physical strength and mental capacity. i. Toxicity: delusions, paranoia, hallucinations, psychosis, vasoconstriction, angina, hypertension, weight loss, tooth decay (meth mouth, deficits in cognition and memory.
